• Food Science and Biotechnology
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• v.17 no.2
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• pp.343-348
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• 2008

In this study, antioxidant activity of methanol extract of Glycyrrhiza uralensis Fisch (GUE) against $H_2O_2$-induced DNA damage in human leucocytcs and cell death in PC12 cells was determined. The effect of GUE on $H_2O_2$-induced DNA damage in human leucocytcs was evaluated by the comet assay, where GUE ($1-50\;{\mu}g/mL$) was a dose dependent inhibitor of DNA damage induced by $H_2O_2$. The protective effect of GUE against $H_2O_2$-induced damage on PC12 cells was investigated by MTT reduction assay and lactate dehydrogenase release assay. A marked reduction in cell survival induced by $H_2O_2$ was significantly prevented by $1-50\;{\mu}g/mL$ of GUE. The enzyme activity of caspase-3 was elevated in $H_2O_2$-treated PC12 cells, while preincubation with GUE for 30 min inhibited $H_2O_2$-induced caspase-3 activation in a dose-dependent manner. In conclusion, GUE ameliorates $H_2O_2$-induced DNA damage in human leucocytes and has neuroprotective effect by preventing cell death in PC12 cell, suggesting that GU may be a potential candidate for novel therapeutic agents for neuronal diseases associated with oxidative stress.

• Toxicological Research
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• v.7 no.2
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• pp.157-163
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• 1991

The effect of patulin, a mycotoxin, on the growth of Escherichia coli cell was investigated. E. coli cell elongation usually shown in SOS-response for DNA repair was induced by 20 mg of patulin per ml. After staining the E. coli chromosome with fluorescence dye(DAPI, 4', 6-diamino-2-phenyl-indole), chromosomal DNA partitioning was not affected by patulin. The observation indicateds that patulin acts as a DNA damaging agent which is effective for E. coli cell elongation introduced by the inhibition of septum formation.

• Toxicological Research
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• v.7 no.2
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• pp.231-238
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• 1991

The pesticide and carcinogen ethylene dibromide(EDB) is metabolized both by cytosolic GSH S-transferase and by microsomal mixed function oxygenase. Cytochrome P-450 IIE1 appears to be major enzyme to metabolize EDB.EDB is activated to a mutagen by enzymatic conjugation with glutathione (GSH). Such activation is an exception to the general mode of detoxification via GSH S-transferase action. The primary DNA adduct (>95) is S-[2-(N7-guanyl)ethyl] GSH and a minor adduct is S-[2-(N7-guanyl)ethyl]cysteine, which is excreted in the urine and may serve as a biomarker of damage.

• BMB Reports
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• v.47 no.4
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• pp.209-214
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• 2014

Ultraviolet B (UVB) radiation induces the production of reactive oxygen species (ROS) that promote apoptotic cell death. We showed that cytosolic $NADP^+$-dependent isocitrate dehydrogenase (IDPc) plays an essential role in the control of cellular redox balance and defense against oxidative damage, by supplying NADPH for antioxidant systems. In this study, we demonstrated that knockdown of IDPc expression by RNA interference enhances UVB-induced apoptosis of immortalized human HaCaT keratinocytes. This effect manifested as DNA fragmentation, changes in cellular redox status, mitochondrial dysfunction, and modulation of apoptotic marker expression. Based on our findings, we suggest that attenuation of IDPc expression may protect skin from UVB-mediated damage, by inducing the apoptosis of UV-damaged cells.

• The Plant Pathology Journal
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• v.17 no.2
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• pp.88-93
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• 2001

Oxidative stress is one of the major limiting factor in plant productivity. Reactive oxygens species (ROS) generated during metabolic processes damage cellular functions and consequently lead to disease, senescence and cell death. Plants have evolved an efficient defense system by which the ROS is scavenged by antioxidant enzymes such as superoxide dismutase (SOD) and ascorbate peroxidase (APX). Attempts to reduce oxidative damages under the stress conditions have included the manipulation of 갠 scavenging enzymes by gene transfer technology. Increased SOD activities of transgenic plants lead to increased resistance against oxidative stresses derived from methyl viologen (MV), and from photooxidative damage caused by high light and low temperature. Transgenic tobacco plants overexpressing APX showed reduced damage following either MV treatment of photooxidative treatment. Overexpression of glutathion reductase (GR) leads to increase in pool of ascorbate and GSH, known as small antioxidant molecules. These results indicate through overexpression of enzymes involved in ROS-scavenging could maintain or improve the plant productivities under environment stress condition. In this study, the rational approaches to develop stress-tolerant plants by gene manipulation of antioxidant enzymes will be introduced to provide solutions for the global food and environmental problems in the $21^\textrm{st}$ century.

• Journal of Community Nutrition
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• v.8 no.4
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• pp.207-213
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• 2006

The present study was conducted to investigate the effect of oolong tea extract on blood glucose level and antioxidant system in diabetic rats. The Sprague-Dawley rats were fed on AIN-76 based experimental diets containing 1 % oolong tea extract for 6 weeks. They were induced to be diabetic by receiving streptozotocin (45mg/kg BW) intramuscularly. Blood glucose, blood and hepatic concentration of vitamins A and E, and antioxidant enzyme activities were measured. Oolong tea extract feeding decreased the plasma glucose in diabetic rats. Dietary supplementation of oolong tea extract did not affect antioxidative enzyme activities such as superoxide dismutase, glutathione peroxidase and catalase in diabetic rats. The plasma level of retinol was increased in diabetic rats by feeding oolong tea extract. Plasma and hepatic levels of ${\alpha}$-tocopherol were higher in diabetic rats fed oolong tea extract. In conclusion, these results suggest that oolong tea extract consumption might reduce the plasma glucose in diabetic rats and protect the oxidative damage from diabetic stress to some extent.

• Journal of Environmental Health Sciences
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• v.27 no.2
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• pp.22-29
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• 2001

To evaluate the cutaneous injury in liver damaged rats by toluene application to the skin, toluene(35mg/㎤) was sequentially applied for 5 days to the dorsal skin of liver damaged rats with $CCl_4$ (6 times ever other day:0.1$m\ell$/100 g body weight-50% $CCl_4$in olive oil). The cutaneous ultrastructural changes were unexoectably not observed in liver from $CCl_4$-treated rats although necrotic liver damage appeared under light microscope. In these animals by the application of toluene to rat skin the cutaneous xanthine oxidase activity was significantly increased(p<0.05), but cytochrome P450 content was not different from that of the control or only $CCl_4$-treated rats. On the other hand, the cutaneous superoxide dismutase and catalase activities in liver damaged animals were significantly respectively(p<0.05, p<0.001), decreased by toluene application to the skin compared with control and especially the former enzyme activity was significantty decreased(p<0.01), compared with that of liver damaged rate rat but glutathione peroxidase, glutathione-S-transferase activities were not significantly different from those of the control or liver damaged rats. Futhermore, the reduced gluathione content of skin was also significantly decreased by toluene application to the liver damaged animals. In conclusion, the great deposits of cerrous peroxide and ultramorphological changes in skin tissue of liver damaged animals by toluene application may be responsible for the oxygen free radical.

• Proceedings of the PSK Conference
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• 2001.04a
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• pp.48-55
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• 2001

When an elongating RNA polymerase encounters DNA damage on the template strand of a transcribed gene it can either be arrested by or be transcribed through the lesion. Lesions that arrest RNA polymerases are thought to be subject to transcription-coupled repair, whereas that damage that is bypassed can cause miscoding, resulting in mutations in the transcript (transcriptional mutagenesis). We have developed a technique using a plasmid-based luciferase reporter assay to determine the extent to which a particular type of DNA base modification is capable of causing transcriptional mutagenesis in vivo. The system uses Escherichia coli strains with different DNA repair backgrounds and is designed to detect phenotypic changes caused by transcriptional mutageneis under nongrowth conditions. In addition, this method is capable of indicating the extent to which a particular DNA repair enzyme (or pathway) suppresses the occurrence of transcriptional mutagenesis. Thus, this technique provides a tool with which the effects of various genes on non-replication-dependent pathways resulting in the generation of mutant proteins can be gauged.

• Journal of the Korean Society of Food Science and Nutrition
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• v.20 no.6
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• pp.527-537
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• 1991

To evaluate an effect of liver xanthine oxidase on the induction of liver damage, carbon tetrachloride (CCl4) was intraperitoneally injected twice at 0.1ml/100g body weight to the rate fed a low (LP)or high protein diet(HP) while the control group fed LP or HP received only olive oil. The changing rate of liver xanthine oxidas activity was compared with that of a free radical generating enzyme, liver aniline hydroxylase and a scavenging enzyme, glutathions S-transferase activity between the rate fed a LP and those fed HP, and the two groups treated with CCl4. Concomitantly, the degree of liver damage which could be considered as the paramete for CCl4 metabolism in case of CCl4-intoxicated animal was observed in the present experimental conditions and the effect of allopurinol, xanthine oxidase inhibitor, on the CCl4-toxicity of rate liver was alos demostrated. On the other hand, the comparative effect of actinomycin D on the liver and serum xanthine oxidase of CCl4-treated rats fed HP with that of those fed LP and the kinetics of purifed liver enzyme from the liver of CCl4-treated rats fed HP was also compared with that of those fed LP to clarify the differences of xanthine oxidase activity between two groups. The increasing rate of liver weigth/body wt, serum levels of ALT and the decreasing rate of hepatic ALT activity and protein contents to each control group were higher in CCl4-treated rats fed HP than those fed LP. Under the animal models as indentified by the present data herein, the liver xanthine oxidase activity was higher in CCl4-treated rats fed HP than those fed LP, and the control group fed HP also showed the much higher activity xanthine oxidase than that fed LP, whereas there were no differences in the activity of hepatic aniline hydroxylase and glutathions S-transferase between the two group treated with CCl4. Although the hepatic aniline hydroxylase activity was somewhat higher in the rats fed HP than those fed LP, the increasing rate of liver xanthine oxidase to the rats fed LP was higher in those fed HP than that of liver aniline hydroxylase. The degree of liver damage identified such as liver weight and serum ALT activity was less in the CCl4-treated rats pretreated with allopurinol. These results suggest that even a system at which xanthine oxidase acts as well as the drug metabolizing enzyme may influence the acelatin of CCl4 metabolism. In addition, the purified liver xanthine oxidase from CCl4-treated rats fed HP showed decreased Km value when compared to its control group. The Km value of liver xanthine oxidase of CCl4-treated rats fed LP showed a similar Km value with its control group. Furthermore, the decreasing rate of liver and serum xanthine oxidase acitivity in CCl4-treated rats pretreated with actinomycin D to the CCl4-treated rats was higher in rats fed HP than in those fed LP. These results suggest that the inductino of xanthine oxidase in CCl4-treated rats fed HP may be greater than in those fed LP.

• Journal of Ginseng Research
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• v.27 no.1
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• pp.11-16
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• 2003

In this study, we investgated the effect of Red Ginseng (KRG) on liver damage induced by carbon tetrachloride (CTC) and galactosamine (GalN) in rats using indicator enzymes such as serum alanine/aspartate aminotransferases, sorbital dehydrogenase, lactate dehydrogenase, and ${\gamma}$-glutamyltransferase. Treatment of KRG restored these enzyme activities to near normal level compared to CTC or GalN treatment alone. Treatment of KRG also enhanced hepatic microsomal enzyme system, malondialdehyde formation, and depletion of reduced glutathione content, which were reduced by CTC or GalN. We also found that the decreased activities of glutathione S-transferase and glutathine reductase but not ${\gamma}$-glutamycysteine synthetase after KRG treatment restored to normal level. These results indicate that KRG has potent therapeutic activity against CTC- and GalN-induced hepatotoxicity in rat.